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6-Clinical Nutrition 1 > Nutrition and Cancer(s) > Flashcards

Nutrition and Cancer(s) Flashcards

1
Q

What is cancer?

A

uncontrolled growth of abnormal cells in the body

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2
Q

What are some characteristics of cancerous cells? (7)

A

– Escape normal growth signals
– Can replicate indefinitely, can form tumors
– Can avoid programmed cell death (apoptosis)
– Can alter energy metabolism
– Can avoid immune surveillance
– Can invade other tissues (metastasis)
– Can develop a blood supply (angiogenesis)

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3
Q

What are some synonyms of cancer?

A

malignant tumors, neoplasms, carcinoma

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4
Q

What are benign tumors?

A

not cancerous, do not invade and metastasize

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5
Q

What is the etymology of cancer?

A

“Cancer”is from the latin cancri = crab and the greek

carcinos = crawfish

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6
Q

What does Prefix“onco-”andsuffix“-oma” mean?

A

malignant massor = tumour
– oncology = science that studies cancer
– ex: melanoma = cancer of the skin

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7
Q

What is the 3-step classic view of carcinogenesis?

A

Initiation –> DNA damage
Promotion –> initiated cells proliferate
Progression –> preneoplastic cells develop into invasive tumors

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8
Q

What is the multistage modern view of carcinogenesis?

A
  • mutations inactivates tumor suppressor genes
  • cells proliferate
  • mutation inactivates DNA repair gene
  • mutation of proto-oncogene creates an oncogene
  • mutation inactivates several more tumor supressor genes
  • cancer
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9
Q

What are proto-oncogenes?

A

promote cell growth and division

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10
Q

What are tumor supressor genes?

A

inhibit cell growth and survival

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11
Q

What are some strategies to block carcinogenesis?

A

anti-initiation strategies

anti-promotion/progression strategies

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12
Q

What are anti-initiation strategies? (4)

A
  • alter carcinogen metabolism
  • enhance carcinogen detoxification
  • scavenge electrophiles/ROS
  • enhance DNA repair
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13
Q

What are anti-promotion/progression strategies? (6)

A
  • scavenge ROS
  • decrease inflammation
  • suppress proliferation
  • enhance apoptosis
  • enhance immunity
  • discourage angiogenesis
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14
Q

What are the components of gene expression?

A
  • genotype
  • penetrance
  • epigenetics
  • phenotype
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15
Q

What is genotype?

A

an individual genetic structure based on his/her DNA

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16
Q

What is phenotype?

A

expression of the genotype: observable characteristics

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17
Q

What is penetrance?

A

the power at gene would be expressed

if we have a certain gene mutation and if it has high penetrance then it will have an affect on the phenotype

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18
Q

What is epigenetics?

A
  • Modification of gene expression rather than alteration of the genetic code itself.
  • Environment including nutrition
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19
Q

What is a mutation? What are the types? Give example

A

structural change in the base pair sequence of DNA
– Inherited: eg. BRCA1 gene ↑ risk of breast and ovarian cancer
– Due to exogenous factors

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20
Q

What is a polymorphism?

A
  • the presence of genetic variation within a population, upon which natural selection can operate
  • structure of the gene varies among individuals (weaker but more common than mutations)
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21
Q

What is a single nucleotide polymorphism? (SNIPs)

A
  • a variation in a single base pair in a DNA sequence.

- may affect the response to exposures

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22
Q

What are epigenetic changes? Give examples

A

affect gene structure, function and expression
– DNA methylation (hypermethylation of the promotor region of tumor suppressor genes → silencing)
– Acetylation of the histones → affects chromatin folding

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23
Q

What are nutritional genomics and proteomics?

A

interactions between diet and genes and their products

bioactive food components that can act in the gene expression

most of the effect will happen after the genomic DNA

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24
Q

What are the major contributors of cancer?

A

tobacco 30%
diet & obesity 30%
genetic background 5%
lack of exercise 5%

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25
Q

Give examples of nutrients affecting gene functions (5) and explain each

A

• Oxidative damage to DNA may be:
–Increased by carcinogens found in foods, polyunsaturated fatty acids, iron
– Decreased by antioxidant nutrients (Vit. C&E) or cofactors in antioxidant enzymes (selenium, copper)

  • Direct role of folate in DNA synthesis, repair and methylation
  • Vitamins A and D interact with promoter regions of many genes, and regulate cell proliferation and differentiation
  • A group of nuclear receptors (PPARα) is activated by oxidized fats
  • Catechins (found in green tea, apples and chocolate) and flavonoids affect gene expression in cell culture
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26
Q

What are possible roles of diet on carcinogenesis? (8)

A

Bioactive food components can affect:

  • cell growth cycle
  • DNA repair
  • Cell differentiation
  • Hormone regulation
  • Carcinogen metabolism
  • Inflammatory response
  • Apoptosis
  • Cell growth cycle
27
Q

indicence vs prevalence ?

A

incidence - when you are diagnosed (counting the new cases of cancer at a certain time)
prevalence - overall number

28
Q

Why is cancer incidence adjusted for age and population growth?

A

as we age we tend to develop more cancer (the risk is higher)

so we have to take that into account when we say incidence

and we need to take into consideration the population growth

regression will do the adjustment for both

incidence of all cancers in blues line but if we adjust with age (decreases) and population (the overall incidense didn’t increase)

29
Q

What are the trends by cancer type in men?

A
  • lung is decreasing from the antismoking
  • colorectal is stable but the mortality is decreasing
  • bladder
  • colorectal and prostate are decreasing but less compared to others
30
Q

What are the trends by cancer type in women?

A
  • breast is the most prevalent cancer
  • lung cancer has increased in women bc the women started to smoke later than men bc it was not socially acceptable in the 50s then we see mortality later on increasing and not it is stabilized
  • breast cancer is decreasing
31
Q

Cancer incidence in developed vs. developing countries

A

liver in developed countries is less bc there are less viruses than the undeveloped ones

western types of cancers associated with western type living

32
Q

Epidemiology of diet and cancer: what are the critical questions?

A
  1. Which dietary factors are important determinants of human cancer?
  2. What is the nature of the dose-response relationship?
    - Risks within the range of intakes actually consumed?
    - Populations may already be consuming sufficient amount of protective factors
  3. What is the temporal relationship?
33
Q

What are some design of studies addressing diet and cancer from weak to strong association? (4)

A
  • Descriptive
  • Case-control
  • Prospective cohort
  • Interventional
34
Q

Describe descriptive studies

A

Cancer rates in populations having different diets are compared.

35
Q

Describe Case-control studies

A

Earlier diets reported by patients with a specific type of

cancer are compared with matched controls without cancer.

36
Q

Describe Prospective cohort studies

A

Incidence of cancer is compared in persons whose diets (and other factors) are determined before follow-up begins.

37
Q

Describe Interventional studies

A

Incidence of cancer in 2 groups randomized to specific interventions is compared.

38
Q

What are the limitations of descriptive studies? (3)

A
  • Diet is only one of many variables.
  • Nutrient intake data are difficult to collect.
  • Best used to generate hypotheses.
39
Q

What are the limitations of Case-control studies? (3)

A
  • Possible recall bias &
  • Selection bias
  • Proxy respondents with rapidly fatal CA
40
Q

What are the limitations of Prospective cohort studies? (2)

A
  • Thousands of people need to be enrolled and health monitored for many years for statistical power
  • Difficult for rare types of CA
41
Q

What are the limitations of Interventional studies? (4)

A
  • Adherence to dietary changes is difficult
  • Blinding is often not possible
  • optimal dosages need to be ascertained
  • duration is unknown and may be long
42
Q

What are the research approaches? (4)

A
  • Dietary intake data often collected using FFQ → represent usual diet over long periods, adequate for large populations
  • Biochemical indicators may be useful for some nutrients (serum oxidative markers, 25(OH)D, …) but not for others (total fat, fiber, sodium, retinol…)
  • More systematic reviews and meta-analysis → limited by possibility of selective publication of positive results, difficulty in combining dietary data and control of covariates.

Epidemiological studies should be viewed as complementary to metabolic, animal, and in vitro mechanistic studies.

43
Q

What are the effects of energy balance, growth rates, obesity on cancer?

A

• The rate of cell division is influenced by energy balance and growth rates → could ↑ replication of initiated cells
• Energy restriction reduces development of cancer
• In humans, growth rates and body size are indicators of energy balance:
– Adult height reflects pre-adult nutrition, adult weight reflects positive balance later in life
• Rapid growth rates before puberty play an important role in future risk of breast and perhaps other CA
• Adult obesity is associated with CA of the colon, kidney, pancreas, esophagus, endometrium, gall bladder, liver
• Obesity and breast CA: greater risk only after menopause

—> Excess weight (and factors related to elevated insulin and IGF-1) could account for one third of CA known to be influenced by nutrition.

44
Q

What are the effects of dietary fat on cancer?

A
  • Several animal studies showed that diets high in fat promote tumor growth, but independent effect from energy intake?
  • Large international differences in breast, colon, endometrium, prostate CA correlate with animal fat intake per capita.
45
Q

What are the effects of dietary fat on breast cancer?

A

• In 65 counties of China with dietary fat intake of 6%-25% of energy → no association with CA mortality. In women consuming 25% → CA rates were below those in US women with same fat intake –> other factors are involved
• Pooled analyses of prospective studies → no association (with fat intake range 20-45% of energy, mostly post-menopausal)
• From one large prospective study: positive association between animal fat and premenopausal breast CA
• Intervention trials of low-fat diet → do not support a benefit (even higher risk was found in one trial!)
• Type of fat:
- Relatively low rates of breast CA in southern European countries associated with use of olive oil (but confounded by whole Mediterranean diet)

46
Q

What are the effects of dietary fat on colon cancer?

A
  • Case-control studies have shown association with intake of fat but,
  • Large prospective studies do not support an association with fat (poly, mono or saturated) that is independent from energy intake.
  • In trial of low-fat diet: no effect was observed

—- Colon CA may be more related to excess weight and low physical activity than dietary fat.

47
Q

What are the effects of Red meat and processed meat on cancer?

A

associations with stomach, colon and rectum CA

– From meta-analysis: 12-17% increase in (possible) risk of colon CA with 100g -increment of red meat intake daily; 49% increased (probable) risk with 25 g-increment of processed meat daily

Potential mechanisms:
– Preservatives (nitrites+salt) and methods of cooking should be considered
• Frying, broiling, grilling → polycyclic aromatic hydrocarbons and heterocyclic amines
– Heme promotes the formation of N-nitroso compounds (nitrosamine)

Role of animal fat? → implications in recommendations of eating lean meat

48
Q

What are the effects of dairy products on cancer?

A

– ↓ risk of colon CA (benefits from calcium, possibly vitamin D)

49
Q

What are the effects of fruits and vegetables on cancer?

A

– contain many phytochemicals with potential anti-carcinogenic properties
• Some promising specific associations:
– Lycopene-containing foods and prostateCA
– Cruciferous vegetables and several CA sites
– Allium vegetables and stomach CA
– Folate-rich F&V and colon CA
– Citrus fruits and lung CA

50
Q

What are the effects of dietary fibers on cancer?

A

• low rates of colon CA with high fiber intake (and stool bulk)
• Proposed mechanisms:
– dilute or bind potential carcinogens,
– limit contact with mucosa by speeding transit,
– alter colonic flora,
– reduce pH,
– serve as substrate to flora producing short-chain fatty acids, e.g. butyrate which has anti-proliferative effect.

51
Q

What are the effects of dietary alcohol on cancer?

A

• Known cause of CA of the oral cavity, larynx, esophagus, and liver especially when combined to cigarette smoking
• Proposed mechanism:
– direct contact and toxicity in the liver
• Substantial evidence from cohort studies support a role to increase risk of breast and colon CA (with ≈2 drinks/day).
• Proposed mechanism:
– “anti-folate”effect of alcohol in a methyl-poor diet (high alcohol, low folate, low methionine)
– High intakes of folate reduces the risk of breast CA associated with alcohol

52
Q

What are the effects of dietary calcium on cancer?

A

• Evidence for calcium to reduce risk of colon CA
– proposed mechanisms: by binding toxic secondary bile acids and ionized fatty acids to form soaps in the lumen, or reducing proliferation and inducing apoptosis in the mucosal cells.
– Threshold of 700-800 mg/day for beneficial effects

  • Intervention trials confirmed protective effect of calcium in patients with history of colon adenoma.
  • Recommendation is to reach calcium RDA ideally with foods, then supplements if needed (ACS 2012 still recommends that men should not exceed RDA, but may be revised)
53
Q

What are the effects of vitamin D on cancer?

A

• Interest generated by observations of low risks of breast, colon and prostate CA in populations with greater sun exposure.
• Some evidence support a role for reducing colorectal CA
– Circulating levels of 25 (OH) D are generally inversely related to colorectal CA in prospective studies
– Vitamin D dietary intake is also inversely related
• Data for other types of cancer are less consistent
• Recent evidence suggests that vitamin D might be important to limit cancer progression
• Large studies ongoing

54
Q

What are the effects of Vitamins C, E &

selenium on cancer?

A

• Vit. C & E: potential roles in reducing cancer risks through antioxidant properties by neutralizing reactive oxygen species (ROS) that cause DNA damage.
• But, epidemiological studies and intervention trials have not consistently supported a role in cancer risk.
• Selenium:
– seleno proteins (glutathione peroxidases) defend against oxidative stress
– Selenium content of food is unreliable, biomarkers are used
– Se+vit E supplements (SELECT trial): no decrease in prostate CA
• No supplements recommended

55
Q

What are the effects of Folate on cancer?

A

• Low folate intake has been linked with higher risks of colorectal, breast and possible cervical CA
– folate in involved in DNA methylation, repair and synthesis
• Long-term use of folic-acid containing multivitamin supplements was associated with 20-70% reduced risk of colon CA
• Intervention trials do not support a beneficial role of supplemental folic acid at 0.5 or 1 mg/day
– Even increased recurrence of adenomas –> supplements may be harmful for those with colon CA and adequate folate intake
• No supplements recommended

56
Q

What are the effects of β-carotene on cancer?

A

• From early observation that increased lung CA risk was associated with low vitamin A intake, 4 major trials of β-carotene supplementation were initiated (1990’):
– 2 resulted in null effects, even after 12years
– 2 reported increased risk in smokers and other adverse effects especially when combined with alcohol (1 study was stopped before the end)

Lack of prior knowledge on pharmacokinetics of β-carotene and multiple interactions with other factors from animal research.

57
Q

What is associated with decreased cancer risk in convincing level of confidence?

A

Physical activity (colon)

58
Q

What is associated with increased cancer risk in convincing level of confidence?

A
  • Overweight & obesity (many CA)
  • Alcohol (oral cavity, pharynx, larynx, esophagus, liver,
    breast)
  • Processed meat (colorectal)
59
Q

What is associated with decreased cancer risk in probable level of confidence?

A
  • Physical activity (breast)
  • Dairy products and calcium
    (colon)
  • Whole grains and fiber (colon)
  • Coffee (liver and uterus)
60
Q

What is associated with increased cancer risk in probable level of confidence?

A
  • Red meat (colorectum)

- Salt preserved foods (stomach)

61
Q

What is associated with decreased cancer risk in Limited - suggestive level of confidence?

A
  • foods containing carotenoids, foods containing vitamin C = fruits and vegetables (oral cavity, oesophagus, stomach, colorectum)
  • Fish, vitamin D,
62
Q

What is associated with increased cancer risk in Limited - suggestive level of confidence?

A
  • Grilled + barbecued meat and fish (heterocyclic amines, polycyclic aromatic hydrocarbons) nitrosamines (from heme),
63
Q

What is associated with decreased cancer risk in Limited-no conclusion level of confidence?

A

omega-3 FA, carotenoids, vitamins B6, B12, folate, C, D, E, Se, non- nutrient plant constituents, garlic, soy, sugar, tea, ….

64
Q

Summary of Recommendations - American Cancer Society 2012

A

• Achieve and maintain a healthy weight throughout life.
• Be physically active.
• Eat a healthy diet, with an emphasis on plant foods.
– Choose foods and drinks in amounts that help you get to and maintain
– Limit how much processed meat and red meat you eat.
– Eat at least 2 1⁄2 cups of vegetables and fruits each day.
– Choose whole grains instead of refined grain products.
• If you drink alcohol, limit your intake.
– Drink no more than 1 drink per day for women or 2 per day for men.

6-Clinical Nutrition 1 (21 decks)

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